Yang Kunqiu, Yin Jiuheng, Sheng Baifa, Wang Qimeng, Han Bin, Pu Aimin, Yu Min, Sun Lihua, Xiao Weidong, Yang Hua
Department of General Surgery, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, P.R. China.
Mol Med Rep. 2017 May;15(5):3019-3026. doi: 10.3892/mmr.2017.6368. Epub 2017 Mar 23.
Keratinocyte growth factor (KGF) stimulates intestinal epithelial cell proliferation upon binding to the KGF receptor (KGFR). The activated aryl hydrocarbon receptor (AhR) serves an important role in the development of tissues by promoting the expression of AhR receptors, which can regulate cell proliferation. In the present study, the signaling pathway between AhR and KGFR in investigated with regards to KGF‑induced intestinal epithelial cell proliferation. Male C57BL/6J wild type and AhR‑/‑ mice, were randomized into four groups: Control, KGF, AhR‑/‑ + KGF and AhR‑/‑ (n=6 per group). The small bowel was harvested on day 5 post‑treatment. LoVo cells were used to study signaling pathways in vitro and were divided into the following four treatment groups: DMSO, KGF, KGF + small‑interfering (si)AhR and siAhR. In vivo, knockdown of AhR mRNA transcripts may abolish KGF‑induced intestinal epithelial cell proliferation. Furthermore, KGFR expression was downregulated following knockdown or silencing of AhR expression in vivo and in vitro. The present study identified that the transcription factor E2F1 could regulate KGFR expression, and that siAhR treatment led to reduced expression of E2F1 in the nucleus and inhibited KGF‑induced cell proliferation. In conclusion, the current results demonstrated that the AhR‑E2F1‑KGFR pathway is involved in KGF‑induced intestinal epithelial cell proliferation.
角质形成细胞生长因子(KGF)与KGF受体(KGFR)结合后可刺激肠道上皮细胞增殖。活化的芳烃受体(AhR)通过促进AhR受体的表达在组织发育中发挥重要作用,AhR受体可调节细胞增殖。在本研究中,针对KGF诱导的肠道上皮细胞增殖,研究了AhR与KGFR之间的信号通路。将雄性C57BL/6J野生型和AhR基因敲除小鼠随机分为四组:对照组、KGF组、AhR基因敲除 + KGF组和AhR基因敲除组(每组n = 6)。在治疗后第5天采集小肠。使用LoVo细胞在体外研究信号通路,并将其分为以下四个处理组:二甲基亚砜(DMSO)组、KGF组、KGF + 小干扰(si)AhR组和siAhR组。在体内,敲低AhR mRNA转录本可能会消除KGF诱导的肠道上皮细胞增殖。此外,在体内和体外敲低或沉默AhR表达后,KGFR表达下调。本研究确定转录因子E2F1可调节KGFR表达,并且siAhR处理导致细胞核中E2F1表达降低,并抑制KGF诱导的细胞增殖。总之,目前的结果表明AhR - E2F1 - KGFR信号通路参与KGF诱导的肠道上皮细胞增殖。